RESUMEN
Gestational diabetes mellitus (GDM) is the most common metabolic complication in pregnancy, which affects the future health of both the mother and the newborn. Its pathophysiology involves nutritional, hormonal, immunological, genetic and epigenetic factors. Among the latter, it has been observed that alterations in DNA (deoxyribonucleic acid) methylation patterns and in the levels of certain micro RNAs, whether in placenta or adipose tissue, are related to well-known characteristics of the disease, such as hyperglycemia, insulin resistance, inflammation and excessive placental growth. Furthermore, epigenetic alterations of gestational diabetes mellitus are observable in maternal blood, although their pathophysiological roles are completely unknown. Despite this, it has not been possible to determine the causes of the epigenetic characteristics of GDM, highlighting the need for integral and longitudinal studies. Based on this, this article summarizes the most relevant and recent studies on epigenetic alterations in placenta, adipose tissue and maternal blood associated with GDM in order to provide the reader with a general overview of the subject and indicate future research topics.
Asunto(s)
Diabetes Gestacional/genética , Epigénesis Genética/genética , Tejido Adiposo/metabolismo , ADN/química , Metilación de ADN/genética , Diabetes Gestacional/metabolismo , Epigénesis Genética/fisiología , Epigenómica/métodos , Femenino , Humanos , MicroARNs/genética , Placenta/metabolismo , Embarazo , Mujeres EmbarazadasRESUMEN
AIM: The objective of this review is to describe the immunological mechanisms which facilitate maternal tolerance at the maternal-placental interface, and to discuss how these mechanisms are disrupted in pre-eclampsia. METHODS: A literature review was performed based on the analysis of papers available on PubMed. The most important and relevant studies regarding the immunological mechanisms which facilitate maternal tolerance in healthy pregnancy and pre-eclampsia are presented in this article. RESULTS: The maternal-placental interface is the site where the immune tolerance begins and develops. Within the innate immunity, natural killer cells, macrophages and dendritic cells play a pivotal role in tolerance through regulation of inflammation. On the other hand, within the adaptive immunity, the correct increase of regulatory T cells is crucial for ensuring immune tolerance toward placental cells. Disturbances in maternal tolerance can lead to the appearance of pregnancy complications such as pre-eclampsia, which has a considerable impact on perinatal morbidity and mortality. CONCLUSION: Our partial knowledge of immunological mechanisms involved in tolerance at the maternal-placental interface indicates that pre-eclampsia is characterized by alterations of this maternal immune tolerance, which could represent the origin of the disease.